The results revealed that APC co-inhibition, interleukin-6/Janus kinase/signal transducer and activator of transcription 3 (IL6/JAK/STAT3) signaling, Toll-like receptor (TLR) pathway, nuclear factor–kappa B (NF-κB) signaling pathway, complement and coagulation cascades, and ferroptosis were enriched, while checkpoint, cytolytic activity, HLA, T-cell co-inhibition, T-cell co-stimulation, and necrosis were inhibited in the sepsis samples compared with the control samples (Figure 8A). The gene discussed is NFKB1; the disease is Sepsis.